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Wound Healing 43

External pressure will impede blood flow when it exceeds capillary
Tissue Injury pressure. In the skin, midcapillary pressure is approximately 20 mm
Hg. In contrast, the forces of compression exerted on the overlying
bony prominence, such as the ischial tuberosity in a recumbent person,
can be as great as 2,600 mm Hg. This amount of external pressure
produces venous and lymphatic obstruction, which increases total
Acute Repeated Trauma, Infection,
Inflamation Hypoxia, Ischaemia, Malnutrition tissue tension and may progress to arterial occlusion. As a consequence
of tissue ischaemia, toxic metabolites accumulate in the tissue spaces
and are a major source of noxious stimuli. In normal individuals,
such noxious stimuli signal a sense of discomfort and pain. With an
Neutrophil Proteases Activation of Chronic Imflammation intact neurological system, the response to pain is an instant change in
Macrophages posture, which relieves the pressure and reverses the adverse metabolic
changes induced by ischaemia. Intermittent relief of pressure as high as
240 mm Hg minimises the tissue damage, and demonstrates the value
Activation of   Neutrophil of intermittent postural change as an effective means of protection from
30
Debridement Growth Factors Macrophages Infiltration pressure-induced necrosis.
Muscle and subcutaneous tissues are more susceptible to pressure-
induced injury than is the skin. Fixation of the skin by an unyielding
  Inflammatory   Reactive fascia also predisposes it to damage. The friction between the skin and
Proliferation Cytokines Oxygen Species the bed sheet when a patient is dragged across the bed can remove the
Fibroplasia protective outer layers of the stratum corneum, thereby accelerating
the onset of ulceration. Shearing forces generated in the subcutaneous
tissue due to this friction can also cause stretching and angulation of
Homeostatic Balance of   Matrix Degrading Proteases vessels, leading to thrombosis and ischaemia.
Proteases and Inhibitors Protease Inhibitors
Pathobiology of Chronic Wounds
In normally healing wounds, acute inflammation with neutrophil infil-
tration brings neutrophil-derived matrix protease enzymes to debride
Epithelization Excessive Matrix Degradation the wound and pave the path for new tissue deposition, remodelling,
Matrix Deposition Degradation of Growth Factors and epithelisation. The regulatory processes that prevent excessive
Angiogenesis Impaired Epithelization matrix degradation include various protease inhibitors derived from the
Tissue Remodeling
serum or secreted by cells at the wound site. An optimal mix of various
growth factors, matrix-degrading enzymes, and their inhibitors create a
physiologic environment for normal healing.
Normal Wound Healing Chronic Wound In chronic wounds, the smoothness and orderliness of the healing
process is disrupted by some underlying abnormality that prolongs
the inflammatory phase and produces a cascade of tissue responses
Source: Nwomeh BC, Yager DR, Cohen IK. Physiology of the chronic wound. Clin Plast Surg that perpetuates the nonhealing state (Figure 8.6). Repeated trauma,
1998; 25(3):341–356.
Figure 8.6: Pathophysiology of chronic wounds: the final common pathway. foreign bodies, pressure necrosis, infection, ischaemia, and tissue
hypoxia also amplify the chronic inflammatory state characterised
by excess neutrophils, macrophages, and lymphocytes. Fragments
wounds require surgical procedures such as multiple debridements, of dead tissue, bacterial products, and foreign bodies are powerful
skin grafting, or flap coverage to facilitate healing. Chronic wounds chemoattractants sustaining a continued influx of inflammatory cells,
27
in African children are often the outcome of poorly treated and infected which in turn produce a variety of growth factors, cytokines, and
traumatic wounds and chronic fungal and mycobacterial infections. matrix-degrading enzymes. Among the most potent of these enzymes
A detailed discussion of these chronic infections is beyond the scope are elastase (Figure 8.7) and the matrix metalloproteinases, which are
of this chapter. Chronic wounds due to diabetes and venous stasis are present in large amounts in chronic wounds. 31
more common in adult patients. Chronic pressure ulcers are common, Given the low levels of protease inhibitors in these wounds, the
and are used in the next section as examples to explain some of the proteolytic enzymes gain the upper hand in degrading all protein
pathophysiological events in chronic wounds. elements found in the tissue, including collagen, fibronectin, and
Pressure Ulcers growth factors. Under these conditions, matrix deposition does not
The term “pressure ulcer” is preferred to the older term “decubitus gain a foothold, and epithelialisation proceeds slowly. It is quite clear
how such a scenario can create a vicious cycle capable of perpetuating
ulcer”, which was derived from the Latin word dêcubitus, meaning wound chronicity. Therefore, any effective intervention must include
“lying down, being bedridden”. These ulcers are characterised by deep a strategy for disrupting this cycle and setting the wound on a
tissue necrosis and loss of volume that is disproportionately greater permanent path toward healing. Wound debridement can achieve this
than the overlying skin defect. 28 objective by removing the proteolytic triggers and restoring a wound
Pressure ulcers are serious and frequent occurrences among microenvironment that favors healing.
children who are immobile and debilitated, including those who have
been hospitalised for a long period. Patients with spinal cord injuries Principles of Therapy
are particularly vulnerable to the formation of pressure ulcers. Several Identifying and treating all the factors that negatively impact wound
primary aetiological factors are important in the formation of pressure healing requires detailed patient evaluation and careful thought.
ulcers. Pressure over bony prominences is a key factor, but shear Ensuring good nutrition and adequate systemic and peripheral perfu-
forces, friction, and moisture are also important in the development of sion are key to promoting wound healing. Treatment of underlying
pressure ulcers. 29 medical problems that may affect healing is also important.